Chronic Kidney Disease

Pyridoxamine or Pyridoxal-5-Phosphate: Potent Kidney Defense

The formation of advanced glycation end-products (AGE's) is a well-established factor in the onset and progression of kidney disease. Nutrients that have been conclusively shown to mitigate the effects of these lethal agents constitute a front line, low-cost intervention.

A formidable AGE antagonist is the vitamin B6 compound pyridoxamine. A plethora of research confirms its power to halt formation of AGE's (Voziyan 2005; Ahmed 2007; Williams 2006). Evidence has also emerged that pyridoxamine drastically limits formation of equally deadly advanced lipoxidation end-products (ALE's)—another catalyst for kidney disease (Alderson 2004; Metz 2003(a,b)).

A team of biochemists at the University of South Carolina were able to show that pyridoxamine traps the reactive molecules formed during lipid (fat) peroxidation and accompanies them harmlessly into the urine (Metz 2003a; Onorato 2000).

Their colleagues subsequently found that neutralizing AGE's and ALE's can prevent kidney disease and lipid profile abnormalities in diabetic rats (Degenhardt 2002). They found that rats supplemented with pyridoxamine had lower levels of albumin (protein) in their urine, lower plasma levels of the waste product creatinine, and less dramatically elevated blood lipids than the placebo-treated rats, all directly related to the reduction of AGE/ALE's.

They subsequently examined whether similar results could be obtained in non-diabetic rats (Alderson 2003). Three groups of rats were studied:

Lean (healthy)

Obese without treatment

Obese treated with pyridoxamine.

As expected, AGE and ALE formation underwent a two- to three-fold increase in obese, untreated rats as compared to lean rats. Conversely, those increases were absent in obese rats treated with pyridoxamine. Treated rats also experienced a smaller increase in plasma triglycerides, cholesterol, and creatinine levels as compared to the obese, untreated rats (Alderson 2003).

In an equally compelling development, hypertension in the rats treated with pyridoxamine resolved, as did thickening of blood vessel walls. Untreated rats displayed urinary evidence of renal disease (albuminuria) that in contrast had been nearly normalized in supplemented rats. This provides powerful evidence of pyridoxamine’s multi-targeted protective effect against CKD (Alderson 2003).

In 2004, the same research team made a landmark discovery. While studying the relative effects of pyridoxamine (along with a variety of additional natural antioxidants) on the progression of kidney disease in diabetic rats, they decided to examine how these natural compounds stacked up against enalapril, a standard pharmaceutical intervention used to prevent CKD (Alderson 2004). Enalapril is an ACE inhibitor, one of a class of drugs commonly used to control blood pressure and kidney disease.

They found that pyridoxamine therapy was the most effective at preventing the progression of kidney disease, followed by vitamin E and lipoic acid. Enalapril, the prescription drug, proved to be the least effective intervention. Pyridoxamine also limited lipid profile abnormalities as well as the formation of AGE's and ALE's, offering a far broader spectrum of preventive effects than enalapril (Alderson 2004).

Researchers at the University of Miami advanced these findings by treating diabetic mice with both pyridoxamine and enalapril (Zheng 2006). Again they found that pyridoxamine alone provided substantial benefit, cutting albuminuria and damage to the glomeruli (capillaries which carry blood within the kidneys). Combining enalapril with pyridoxamine reduced kidney disease mortality in these animals as well, leading the researchers to suggest that the ACE-inhibitor (enalapril)/pyridoxamine combination might be useful.

A convincing body of research on pyridoxamine therapy in humans with CKD has emerged. In 2007, a team of researchers at Harvard University set out to determine optimal interventions to halt the progression of kidney disease in diabetics (Williams 2007). They conducted two 24-week multicenter placebo-controlled trials in patients with known diabetic nephropathy—treatment of which is known to delay the onset of end-stage renal disease in diabetics. Doses of pyridoxamine ranged from 50 to 250 mg twice daily.

Pyridoxamine significantly inhibited the rise in blood levels of the waste product creatinine, one of the key biomarkers of kidney dysfunction and a predictor of kidney failure. Urinary levels of inflammatory cytokines were also significantly lower in the treated group compared to controls.

Pyridoxamine has been firmly established as a front line, safe, low-cost intervention in CKD caused or exacerbated by AGE's and ALE's. Further, this natural vitamin B6 compound has been shown to significantly improve outcomes of experimental kidney transplants and other forms of kidney disease (Murakoshi 2009; Tanimoto 2007; Waanders 2008).

It therefore borders on the criminal that in January of 2009, the FDA classified this potent, entirely safe CKD therapeutic as a drug, putting it out of reach for many Americans suffering from this deadly condition. No one should be forced to bear the outrageous burden of costly pharmaceuticals and their toxic side effects when a perfectly safe alternative exists.

Fortunately, there is another equally safe option available—another form of vitamin B6 known as pyridoxal-5-phosphate (P5P) that also exerts potent anti-AGE effects. It has been shown to prevent the progression of diabetic kidney disease in pre-clinical models (Nakamura 2007). In fact, as far back as 1988, P5P was used by a German research group to reduce blood lipids in humans with chronic kidney disease (Kirsten 1988).

These statements have not been evaluated by the Food and Drug Administration.
These products are not intended to diagnose, treat, cure, or prevent any disease.

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